Antacid-induced phosphate depletion syndrome presenting as nephrolithiasis.
A 29-year-old insulin-dependent diabetic woman developed phosphate depletion, nephrolithiasis and bilateral ureteric obstruction due to antacid abuse. Unlike previous descriptions of chronic phosphate depletion, myalgia, weakness and bone pain were absent. Biochemical features included hypophosphataemia, hypercalciuria, hypophosphaturia, elevated plasma, 1,25-dihydroxyvitamin D and low plasma intact parathyroid hormone. These abnormalities were corrected when antacid ingestion was reduced and phosphate intake supplemented. We propose that phosphate depletion secondary to antacid abuse caused 1 alpha-hydroxylase activation and elevation of the plasma 1,25-dihydroxyvitamin D level, leading to marked hypercalciuria. Once diagnosed, antacid abuse is a readily reversible cause of hypercalciuria and renal stones. Moreover, antacid-induced phosphate depletion may present with nephrolithiasis in the absence of musculoskeletal symptoms. This report is intended to draw attention to this important cause of renal stone disease.
Harmelin
D L
DL
Royal Melbourne Hospital, Vic., Australia.
Martin
F I
FI
Wark
J D
JD
D000328:Adult; D000863:Antacids / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007669:Kidney Calculi / Q000209:etiology*; D010710:Phosphates / Q000172:deficiency*; D012008:Recurrence; D013577:Syndrome
D000863:Antacids; D010710:Phosphates